Flashcards in Adrenergic / Cholinergic Deck (37):
NMJ blocker by non-depolarization. Competitive antagonist of N AchR
NMJ blocker by depolarization. Agonist for N AchR. Fasciculations follow by phase 1 (depolarization), then phase 2 (desensitization). Resists Achase.
N AchR agonists? (2)
Acetylcholine and nicotine
N+M AchR agonist, resists AchE
N AchR antagonist
M AchR agonists? (3)
Muscarine, pilocarpine (salivary gland and glaucoma), and bethanechol (bladder).
Atropine and scopolamine
M AchR antagonists. Belladonna alkaloids.
Enters cholinergic nerve and prevents vesicle fusion.
Physostigmine and neostigmine
Reversible AchE blockers, physostigmine enters CNS to cure atropine poisoning
Parathion, malathion, sarin
Organophosphates that irreversibly inhibit AchE. Temporarily cured by atropine. Permanently cured by pralidoxime.
Nonselective a and b agonist. At low binds b, at high binds a and b.
a agonist, b1 > b2.
b1 and b2 agonist.
a1 agonist. Raises blood pressure.
b2 agonist. Treats asthma.
a2 agonist. Treats hypertension.
Increase norepinephrine in nerve terminals and potentiate tyramine.
Activates Gq, PLC, DAG and IP3. Vasoconstriction and GI muscle relaxation.
Activated Gs, cAMP increases. Increases heart contractility, rate, AV conduction, and renin release from kidneys.
Activates Gs, cAMP decreases. Vasodilation.
Indirectly increases sympathetic by promoting norepinephrine vesicle fusion.
Ephedrine and Amphetamine
Indirectly activates sympathetic by increasing norepinephrine release.
Cocaine and tricyclic antidepressants
Inhibit norepinephrine uptake.
a1 and a2 antagonist
b1 and b2 antagonist
Thiazide diuretic. Block NaCl symporter in distal tubule. Increased Na, K, Cl excretion. First drug given.
Block NKCC in TAL to increase Na, K, Cl excretion. Used for pulmonary edema and as secondary drug. Interacts with antibiotics and NSAIDS.
Potassium sparing diuretics
Can either act on Na channel or as aldosterone analogue antagonist.
Blocks B1R in heart (decrease HR, contractility, and CO) and in kidney (decrease renin, A2, and TPR)
Alpha 2 agonists
CNS agonists to vasodilate. Very rare cases.
A1 antagonist leads to vasodilation which decreases TPR and MAP. Secondary drug.
CCB in arterial smooth muscle. Blocks L VG Ca channel
CCB blocks calcium entry into myocytes
Vasodilator that activates K channels to hyperpolarize cell and prevent contraction
ACE inhibitor and Kininase inhibitor (raises vasodilator bradykinin). All cleared by kidney and may lead to hyperkalemia. No prego, cough.
At1 blocker, insurmountable competitive antagonist. Hyperkalemia. No prego.